This document discusses gout, a metabolic disease characterized by recurrent attacks of acute inflammatory arthritis caused by elevated uric acid levels in the blood. It defines gout and discusses its pathogenesis, stages, risk factors, clinical features, differential diagnosis, investigations, and treatment. The document outlines that gout results from uric acid crystallizing and depositing in joints due to either overproduction or under excretion of uric acid. It can be diagnosed through testing of synovial fluid, blood, or urine and is treated with medications, diet modification, exercise, and surgery if needed.

1. SHRUTI
PUROHIT
FINAL YEAR

2.  Defination
 Pathogenesis
 Stages Of Gout
 Risk Factors
 Clinical Features
 Differential Diagnosis
 Invetigation
 Treatment

3.  A Metabolic Disease Characterised By Recurrent
Attack Of Acute Inflammatory Arthritis Caused By
Elevated Levels Of Uric Acid In The Blood.
(Hyperuricemia)
 Most Common Rheumatic Disease Of Adulthood.
 The Uric Acid Crystallizes & Deposits In Joints,
Tendons, & Surrounding Tissues As Tophi.
 Podagra Is A Painful Condition Of The Big Toe
Caused By Gout.
 Mainly Affect Big Toe, Also Affects Knees, Ankle,
Wrists, Fingers, Elbow, Toes Of Feet.

5.  2/3 of urate formed each day is excreted
by the kidneys & 1/3 from GI tract.
 Normal adult excrete 500-700mg of uric
acid/day.
 The Purine That A Person Eats & Also
Produced Naturally In Body, Are Metabolized
By The Body.
 Liver Is The Major Site Which Breaks Down The
Purines & Produces A Waste Product Called
Uric Acid.

6.  The Uric Acid Is Released Into The
Bloodstream & Eventually Filtered By The
Kidneys & Excreted In The Urine.
 If Too Much Uric Acid Builds Up Can Form Into
Crystals That Deposit In Your Jts. & Cause
Pain & Inflammation.

8.  Elevated Uric Acid Can Occur From Over
Production Or Under Excretion Of Uric Acid
 Over Production: (PRIMARY GOUT) 10-20%
• Less Common
• Genetic Abnormalities In Enzymes Related
Purine Metabolism
• ↓ Hypoxanthine-guanine Phosphorebosyl
Transferase(hgprt)
• ↑ Phosophoribosyl Pyrophosphate
Synthetase(prpp)

9.  Under Excretion: (SECONDARY
GOUT) 80-90%
• More Common
• ↓ GFR
• Decline In Urinary Excretion Of Uric Acid
 Can Determine By Measuring Urine Uric Acid
• >600mg/24hr Over Production
• <600mg/24hr Under Excretion

10. 4 stages:
 Asymptomatic
Hyperuricemia
 Acute Gout
 Intercritical Gout
 Chronic Tophaceous
Gout

11.  Serum Uate Abnormally High Without
Sign & Symptoms.
 Male > 7mg/Dl
 Female > 6mg/D
 Not Life Threatening & Readily
Treatable.
 Routine Prophylactic Rx Is Not
Required.

12.  The Intervals Between Attacks Of
Gouty Arthritis Are Reffered To As
Intercritical Periods.
 Intercritical Gout Simply Has Gout That
Has Caused Attacks Of Inflammation
In A Jts. In The Past But It Is Not Active
At The Time Evaluating The Pt.

13.  Acute, Self Limiting, Monoarticular
 Painful, Red, Hot, Swollen Accompained By
Fever, Raised ESR
 Usually Resolved Within 2 Weeks If Untreated.
But Recurrent Attacks Are Followed By
Progressive Cartilage & Bone Erosion,
Deposition Of Tophi, Secondary OA, &
Disability Associated With Permanent Restriction
Of Jt. Fun.
 May Occur Even If Serum Urate Is Normal
 Ll>Ul
 Also Present As Tenocynovitis, Bursitis, Cellulitis

14.  Polyarticular Arthritis + Tophi Formation.
 Articular Topheceous Gout May Results In
Destructive Arthropathy & Secondary OA.
 Serum Urate Level > 7mg/Dl.
 Disease Onset At Younger Age ≤ 40yrs.
 Sites Of Tophi:
 Digits Of Hands & Feet
 Helix Of Ear
 Bursa Around Elbow & Knee
 Achilles Tendon

15. o age (>35yr)
o sex (m>f=3:1)
o obessity
o high blood pressure
o injury
o recent surgery
o foods / drinks
o medications(diuretics, levo-dopa,
salicylates, nicotinic acid, cyclosporine)
o genetics (SLC2A9 , SLC22A12, ABCG2)
o medical
conditions(hypothyrodism, dm, pso-
riasis, heart failure, renal transplant, chronic
renal insufficiency, coronary heart disease)
o high protein diet
o life style

16. o Sever Pain At Joint
o Redness & Inflammation
o Fever
o Less Flexibility
o Nodules
o Itchy & Peeling Skin Later

17. Pseudogout (Deposition Of Calcium
Pyrophosphate Dyhydrate)
Septic Arthritis
Rheumatoid Arthritis
Trauma
Psoriatic Arthritis
Bursitis, Cellulitis, Tenosynovitis

18. Lab. Diagnosis
• Evidence Of Monosodium Urate Crystals By Jt.
Aspiration For Definitive Diagnosis
Synovial Fluid Analysis- Arthrocentesis
• Blood Test- Check Serum Uric Acid Level
• Urine Test
Most Uric Acid Disolves In Blood & Travels To The Kidneys, Where It
Passes Out In Urine.
If Body Produces Too Much Uric Acid Or Dosen’t Remove Enough Of
It, Person Can Get Sick

20.  REDIOGRAPHIC DIAGNOSIS

21.  PHARMECOLOGICAL
Rx
• NSAIDs
• Colchicine
• Corticosteroids
• Uricosurics
• Allopurinol
• Xanthine Oxidase
 Other
• Wt.Loss
• Exercise
• Diet(purine Contain
Diet ×)
 Surgical
• Removal Of Tophi
• Joint Fusion
• Joint Replacement

23. 
PHYSIOTHERAPY
 Pain control
 Barce
 Cryotherapy
 Ultrasound(1MHZ,1-
2W/Cm², 3-5min)
TREATMENT
 Rom
 Strenghtening
Ex.

25.  A Seronegative Arthritis Found In Pts. With
Psoriasis.
 It Is A Chronic Disease Charecterized By A
Form Of Inflammation Of The Skin & Jts.
 Classified With Hla-b27 Genetic Factor
Associated Spondyloarthritis.
 Immunologic Factor & Environmental Factor
Also Progress The Disease.
 Males & Femaes Are Equally Affected
 Peak Age Of Onset Between 30-55yrs.

26.  Family history.
 trauma, viral, bacterial
infection.
Signs & symptoms
 Painful,Tendor,Swolloen Jts.
 Hot red jts.-knee, ankle, feet
 Fatigue, morning stiffness
 Pitted nails, LBP

27.  Gouty Arthritis
 Ankylosing Spondyosis
 Rheumatoid Arthritis
INVESTIGATIONS
 Not Specific Diagnostic Test.
 Elevation Of Esr.
 Base On Clinical & Rdiological Basis.

28. New Bone Formation In Distal Jts.
 Lysis Of Terminal Phalanges.
“ Pencil In Cup” Like Appearance.

29.  Nsaids
 Corticosteroids
 DMARDS- Methotrexate,cyclosporine
 Coordinate B/W Rheumatology &
Dermatology

30.  Modalities- Heat, Cold
 Orthotics
 Active & Passive Exercise
 Streatching
 Strengthening